Anxiety disorders are the most common psychiatric diagnosis, affecting as many as 29% of people during their lifetime. In addition to the devastating personal cost of anxiety, the yearly economic cost to society has been estimated to be around 46.6 billion. Major progress has been made in the treatment of anxiety using selective serotonin reuptake inhibitors (SSRIs) and cognitive behavioral therapy (CBT). However, obstacles to their wide-scale use and high remission rates (about 50%) suggest the need for complementary treatment approaches. Computer-based attention bias modification (ABM) treatment, which is brief, cost-effective, and easy to administer, addresses common treatment barriers and targets a key mechanism in pathological anxiety - the threat bias, or exaggerated attention towards threatening stimuli. ABM uses a modified version of the dot probe task to train anxious individuals to redirect attention away from threat. A recent meta-analysis of ABM effects on anxiety documents reductions in anxiety symptom severity, with effect sizes comparable to those for CBT. However, no research has evaluated specific neurocognitive mechanisms underlying ABM's effects on anxiety, nor attempted to identify biomarkers that can predict treatment response. The goal of the proposed project is to conduct the first large-scale RCT of ABM treatment for anxiety that integrates a neural biomarker approach to elucidate neurocognitive mechanisms underlying treatment efficacy and to test whether these biomarkers can identify those individuals for whom remediation of attention dysfunction via ABM will be most effective. Scalp-recorded event- related-potentials will be the biomarker due to their extremely high temporal resolution and sensitivity to automatic and controlled attentional processes that are implicated in ABM. The proposed research will pursue two Specific Aims: Aim 1 will test whether ABM treatment modifies ERP responses to threat in 90 anxious adults. We predict that adults who receive ABM (versus placebo) will exhibit at post-training: (a) significantly larger ERPs indicating increased control of attention to threat (N2/N2pc/P3); and (b) significantly reduced ERPs indicating diminished facilitated attention to threat (P1, P2) - although previous mixed evidence suggests these effects may be less robust than those for controlled attention. We will test the exploratory hypothesis that these changes in ERPs due to ABM will predict reductions in reaction-time based measures of threat bias. Aim 2 will test whether changes in ERPS due to ABM (detailed in Aim 1) are associated with reduced anxiety severity. We predict that changes in ERPs reflecting increased control of attention, and to a lesser degree reduced facilitation of attention to threat will predict amelioration of anxiety and stress reactivity following treatment. We will examine maintenance of treatment effects four months following treatment completion. We will also assess whether ERPS can be used to predict treatment response by testing the exploratory hypothesis that participants showing ERP responses at baseline indicating greater biased attention to threat (greater facilitation (larger P1/P2) and reduced control of attention (diminished N2/N2pc/P3)) will benefit most from remediation of attention dysfunction and thus show greatest reductions in anxiety severity and stress reactivity due to ABM. The proposed research, by integrating neural and behavioral markers, represents a crucial next step in understanding mechanisms underlying plasticity of the threat bias and remediation of anxiety. Such findings have the potential to yield high impact knowledge of the etiology of anxiety disorders, create more targeted, personalized, and cost-effective interventions for anxiety, and help predict individual differences in treatment response.